Treatment for Alzheimer disease by CpG with RVG
Project/Area Number |
26670441
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Neurology
|
Research Institution | Nagoya University |
Principal Investigator |
Mizuno Tetsuya 名古屋大学, 環境医学研究所, 客員准教授 (70335008)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | ミクログリア / アルツハイマー病 / 機能性ペプチド核酸 / RVG-CPG / 脳移行性ペプチド / CpG |
Outline of Final Research Achievements |
Soluble oligomeric amyloid beta (oAb) 1-42 causes synaptic dysfunction and neuronal injury in Alzheimer’s disease (AD). Microglia are involved in AD pathology. Microglia activated with unmethylated DNA CpG motif (CpG), a ligand for toll-like receptor 9, attenuated oAb neurotoxicity. In this study, we developed CpG with a specific target peptide for the brains; ravies virus glycoprotein (RVG). Intraperitoneal (IP) administration of CpG with RVG ameliorated the impairment of associative learning in APP/PS1 mouse model of AD. We propose that CpG with RVG may be an effective therapeutic strategy for inhibiting oAbeta 1-42 neurotoxicity in AD.
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Report
(3 results)
Research Products
(3 results)